Intimal and neointimal fibroplasia leading to late failures of at least 50 percent of arterial reconstructions have been extensively documented, bear striking resemblance to atherosclerosis obliterans, and appear to be hemodynamically dependent. Based upon clinical observations in failed arterial reconstructions, experimental models have been developed in dogs by alteration of local hemodynamic conditions and extensively studied by light and electronmicroscopy for serial changes. Having standardized a number of hemodynamic models, it is planned to perfuse these models in situ with a variety of fluids to learn the role of various components of blood in the development of lesions. The specific stimuli which result in smooth muscle cell migrations may thereby be determined. The role of mitotic division in the development of fibromuscular intimal plaque will be studied by continued use of antimitotic drugs such as colchicine at various stages of evolution of the plaques in arterial autografts and in endarterectomized segments. The relationship of fibrous intimal plaques to compound atherosclerosis will be studied by alteration of lipid profiles in animals with various hemodynamic models.